ObjectiveTo systemically review the efficacy and safety of moxifloxacin for mycoplasma pneumoniae. MethodsSuch databases as PubMed, The Cochrane library (Issue 4, 2014), ISI, CBM, CNKI, VIP and WanFang Data were searched from inception to April 2014 for randomized controlled trials (RCTs) concerning moxifloxacin for mycoplasma pneumoniae. Two reviewers screened literature according to the inclusion and exclusion criteria, extract data, and assess methodological quality of included studies. Then meta-analysis was performed using RevMan 5.2 software. ResultsA total of 16 RCTs involving 1 401 patients were included. The results of meta-analysis showed that:compared with erythrocin or azithromycin, moxifloxacin had higher recovery rate (OR=2.35, 95%CI 1.76 to 3.15, P<0.000 01), higher bacterium negative rate (OR=3.74, 95%CI 1.76 to 7.96, P=0.000 6), and shorter fever clearance time (MD=-1.07, 95%CI -1.43 to -0.71, P<0.000 01); compared with azithromycin alone, moxifloxacin combined with azithromycin had higher recovery rate (OR=1.63, 95%CI 1.09 to 2.42, P=0.02), higher bacterium negative rate (OR=5.78, 95%CI 2.41 to 13.84, P<0.000 1), and shorter fever clearance time (MD=-0.99, 95%CI -1.52 to -0.47, P=0.000 2). In addition, there was a lower incidence of liver damage (OR=0.16, 95%CI 0.04 to 0.72, P=0.02) in patients who took moxifloxacin compared with erythromycin or azithromycin. No significant difference was found in the incidence of gastrointestinal adverse reaction between the two groups. ConclusionMoxifloxacin for mycoplasma pneumonia is more effective than macrolides (erythrocin or azithromycin) with a lower incidence of adverse reaction. Due to limited quantity and quality of the included studies, the above conclusion should be further verified by conducting more high quality, large scale, multicentre RCTs.
ObjectiveTo investigate the effect of azithromycin on chronic obstructive pulmonary disease (COPD) vascular remodeling and its possible mechanism.MethodsEighteen male SD rats were randomly divided into normal control group (group A), model group (group B) and azithromycin intervention group (group C). In group B and group C, the COPD model was established by passive smoking and intratracheal injection of lipopolysaccharide. On the fifteenth day, group C was intragastricly administrated with azithromycin (50 mg/kg) one hour prior to smoking, while group A and group B were given equal amount of normal saline. All the rats were killed 6 weeks later. Hematoxylin-eosin staining was used to observe lung tissue pathological changes and victoria blue + Van Gieson staining was used to observe the pulmonary artery morphology changes. The serum osteopontin (OPN) was determined with ELISA. The protein expression of OPN was measured with immunohistochemistry and OPN mRNA was detected by RT-PCR.ResultsCompared with group A, the degree of pulmonary vascular inflammation and pulmonary vascular remodeling in groups B and C was more serious, but these changes in group C were lighter than those in group B. The serum OPN content, lung tissue OPN protein and OPN mRNA expression in groups B and C were higher than those in group A, while these parameters in group C were lower than those in group B. The content of serum OPN, the expression of OPN protein and OPN mRNA in lung tissue were positively correlated with the degree of pulmonary vascular inflammation and vascular remodeling.ConclusionAzithromycin can alleviate the pulmonary vascular inflammation and pulmonary vascular remodeling in COPD rats, and its mechanism may be related to inhibiting the expression of OPN.